Objective: Recognize the clinical and diagnostic features of diabetes caused by type B insulin resistance and treat with immunosuppressive therapy.Methods: A 27-year-old Asian male with a recent diagnosis of systemic lupus erythematosus (SLE) presented to his primary care physician complaining of a 2-month history of polydipsia, polyuria, unintentional 20-pound weight loss, and darkening of the skin on his posterior neck, back, and axilla. He had no family history of diabetes. The patient was presumed to have type 2 diabetes mellitus and started on oral medications. He continued to have poor glycemic control for 8 months despite treatment with multiple oral hypoglycemic agents (metformin, pioglitazone, sulfonylurea), glucagonlike peptide-1 agonist, and high doses of insulin. Given the history of SLE, hypercatabolic state, and severe acanthosis nigricans on examination, type B insulin resistance was suspected. The diagnosis was confirmed by the presence of high titer of insulin receptor antibodies. The patient was treated with rituximab, cyclophosphamide, and pulse dose steroids per National Institutes of Health protocol.Results: Four months after treatment the glycemic control improved and after 7 months the patient's diabetes went into remission and all the metabolic derangements resolved.Conclusion: Type B insulin resistance is an autoimmune disorder caused by autoantibodies against the insulin receptor. Recognition of this syndrome remains important, because it affects both treatment and prognosis. Our patient responded well to the immunosuppressive regimen with remission of his severe insulin resistance and resolution of the metabolic abnormalities. (AACE Clinical Case Rep. 2016;2:e256-e259) Abbreviations: AN = acanthosis nigricans; ANA = antinuclear antibody; NIH = national Institutes of Health; SLE = systemic lupus erythematosus

Objective: The aim of this study is to analyze the body composition of patients receiving emergent dialysis and compare their body cell mass (BCM) and fat-free mass (FFM) with those of normal subjects. The care of patients receiving sporadic, emergent dialysis treatment is a growing public health concern and the magnitude of muscle wasting that occurs in this population is not known. Design and Methods: We used a cross-sectional design with matching to determine differences in total body potassium - an indicator of both BCM and FFM - between emergent dialysis patients and healthy normal subjects. We studied 22 subjects using a ⁴⁰K counter that measures BCM and FFM and compared them to controls after matching with sex, height and weight. Results: In the matched comparison, BCM and FFM were significantly lower in subjects with end-stage renal disease (ESRD). Unadjusted BCM was 4.7 kg lower and FFM was 8.8 kg lower for those with ESRD compared to those without ESRD (p < 0.001, p < 0.001, respectively). Comparison with unmatched controls who underwent ⁴⁰K analysis also revealed significantly lower BCM (4.1 kg) and FFM (7.7 kg) in the ESRD subjects (p = 0.004). After adjusting for age, height, weight and gender, BCM and FFM were lower by 4.2 and 7.8 kg, respectively (p < 0.001). Repeated observations were available for a subset of ESRD subjects, and the rate of FFM loss over time was significant, with the ESRD subjects demonstrating 2.2 kg per year decline (p = 0.01). Conclusion: We conclude that among other consequences, muscle wasting indicated by decline in BCM and FFM is a significant concern in the growing emergent dialysis population.